Mood symptoms
Depressed, low, or irritable mood
Diminished interest or pleasure
Neurovegetative symptoms
Weight or appetite change (decreased or increased)
Dyssomnia (insomnia, hyposomnia, hypersomnia)
Psychomotor agitation or retardation
Fatigue or loss of energy
Cognitive symptoms
Indecisiveness
Diminished attention or concentration
Feelings of worthlessness/guilt
Feelings of hopelessness
Suicidality (ideation, intent, behavior)
84% of their patients with major depression had at least one comorbid condition
61% had an Axis I disorder
30% had an Axis II diagnosis
58% had an Axis III illness
A lowering of the age of onset, with an increase in the late teenage and early adult years
A persistent gender effect, with the risk of depression consistently two to three times higher among women than men across all adult ages
The suggestion of a recent narrowing in the differential risk to men and women because of a greater increase in the risk of depression among young men
A persistent family effect, with the risk about two to three times higher in first-degree relatives as compared with control subjects, suggesting a genetic predisposition for at least some forms of depression
Current or past hypomania/mania
Current and past treatment and outcomes
History of a substance use disorder
General medical history
Thorough review of symptoms (particularly in elderly patients with a first-time episode)
Personal history (e.g., psychological development, response to life transitions, major life events)
TABLE 6-1 DIFFERENTIAL DIAGNOSIS OF DEPRESSION | ||||||||
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Central measures of neurotransmitter function (e.g., norepinephrine, serotonin, dopamine; glutamate); excitatory amino acids; and neuropeptides, particularly corticotrophin-releasing factor [CRF])
Measures of hypothalamic-pituitary axis function, such as the dexamethasone suppression test, the thyrotropin-releasing hormone test, and growth hormone response to clonidine
Peripheral markers of neurotransmitter receptors (e.g., lymphocyte β-adrenoreceptors, platelet α2-adrenoreceptors, platelet imidazoline receptors, platelet 5-HT2 receptors, phosphoinositol turnover, and a variety of ways of measuring platelet serotonin uptake)
Immunological markers, particularly those involving cytokines and lymphocyte function
Shortened rapid eye movement latency on the electrooculogram
Prolactin response to serotonin enhancers such as D-fenfluramine, chlorimipramine, L-tryptophan, and 5-hydroxytryptophan
Measures of melatonin secretion and turnover
Candidate gene approaches (e.g., FKBP5 gene)
Functional polymorphisms for the 5-HT transporter gene
TABLE 6-2 PRESENTING COMPLAINTS OF DEPRESSION BEYOND THE TYPICAL SYMPTOMS ACROSS THE LIFE CYCLE | ||||||||
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Accuracy of diagnosis
Adequacy of the treatment trial
Antidepressant dose and duration
Cognitive behavioral therapy (CBT) or interpersonal psychotherapy (IPT) trial (e.g., proper technique, number and frequency of sessions)
Sufficient adherence to treatment
Level of recovery
Response
Remission
Functional status
Quality of life
poor response due to a variety of factors other than true treatment resistance.
Increased resistance is determined by successive failures of various antidepressants and electroconvulsive therapy (ECT) (21)
Distinguishing across a continuum from nonresponse, treatment resistance, and chronic resistant depression (22)
Consideration of both the number of failed trials and the optimization of each attempt (23)
Anxiety and sleep-related disorders
Alcohol and other substance use disorders
Pain syndromes
Axis II disorders
Attention-deficit hyperactivity disorder (ADHD)
TABLE 6-3 SUBTYPES OF DEPRESSIVE DISORDER | |
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A patient has a complaint (e.g., insomnia)
The physician determines through questioning that the patient has a full depressive syndrome
The physician rules out medical causes for the depressive syndrome through further history taking, a physical examination, and laboratory tests
The physician must then assess whether the patient has a unipolar or bipolar disorder, because patients with the latter disorder are often first seen with a depressive episode.
The patient’s age—the younger the patient, the greater the chance that the course will be that of a bipolar disorder on longitudinal follow-up
A positive family history for bipolar disorder, particularly in first-degree relatives
A hypomanic phase before the onset of the depressive episode
Antidepressant “misadventures”
Phenomenology
Family history of the illness, especially in firstdegree relatives
Age of onset distributions
Response rates to specific types of therapies
Incidence of positive biological markers (e.g., dexamethasone suppression test [DST] in psychotic depression) (36)
Atypical presentations can be misdiagnosed as a personality disorder, particularly because common and prominent symptoms include irritability, demanding demeanor, and hostility
Psychotic episodes may be misdiagnosed as schizophrenia in younger patients or dementia with paranoia in the elderly
Failure to identify the specific type may delay the most effective treatment
Failure to consider differing natural courses of each type handicaps anticipation of sequelae
A profoundly depressed mood and appearance
Anhedonia
Feelings of helplessness, hopelessness, worthlessness, and guilt
Problems with initial, middle, and terminal (or early morning awakening) insomnia
Significant anorexia, often with appreciable weight loss
Psychomotor retardation or agitation
An absence of mood reactivity
A diurnal variation in the severity of symptoms
Age of onset in the mid-forties
Female-to-male ratio of 2:1
Hypersomnia rather than insomnia
Hyperphagia rather than anorexia
Psychomotor agitation rather than psychomotor retardation
Anxious or irritable mood rather than dysphoria
A younger age of onset than for melancholia, with a mean in the mid-twenties
Female-to-male ratio of about 3-4:1
One has cancer as a punishment from God
One is bankrupt because of fiscal irresponsibility
One is perceived as evil
One has ceased to exist
full neurovegetative syndrome. There are still many questions about this condition, including
Is it a fundamentally different condition than MDD?
Does it share a common pathophysiology or etiology with MDD?
Is it the precursor of a MDD?
Is it the residue of an incompletely remitted MDD episode?
Is it the sequelae of a MDD episode that did not receive prompt and adequate treatment?
Panic disorder, panic attacks
Social anxiety disorder
Obsessive-compulsive disorder
Generalized anxiety
Physical complaints, such as tachycardia, dyspnea, dizziness, flushing, tremor, and sweating
Cognitive complaints, usually characterized as a sense of catastrophic fear of dying, losing control, or going “crazy”
Affective symptoms including terror, heightened arousal, marked anticipatory anxiety, and feelings of despair and failure
Behavioral symptoms, such as social withdrawal, excessive dependency, and phobic avoidance (e.g., agoraphobia)
environmental factors on mood, which have been described for more than two millennia. Although the Seasonal Pattern Assessment Questionnaire (SPAQ) has demonstrated validity as a screening instrument to help identify patients with this disorder, its utility and even the construct of SAD as a diagnosis are questioned by some (43,44,45,46 and 47).
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